The mechanism and physiological function of cell cycle dependent changes in cell surface receptors will be investigated in two different systems: 1. MSH-receptors of melanoma cells; 2. Hapten-binding cell surface immunoglobulins (slg) of myeloma cells. 1. We have previously shown that the expression of MSH receptors in melanoma cells is dependent on the cell cycle; it is maximal in the G2 phase. Our major objective now is to determine the mechanism and physiological role of cell cycle dependency of MSH receptors and to investigate how the responsiveness of melanoma cells to MSH is regulated by growth controls. Cell cycle and MSH-receptor content of melanoma cells, cultured in serum-containing and chemically defined medium will be analyzed by microfluorimetry and flow cytometry of cells, labeled with MSH. The effect of growth controls on the expression of MSH receptors and hormone-induced melanogenesis will be studied. Also, we want to develop a method to prevent cell cycle-dependent evasion of melanoma cells from site-directed (MSH-receptor mediated) chemotherapy of melanomas. 2. We have found that the number of hapten-binding slg (315) changes during the cell cycle of MOPC-315 plasmacytoma cells. We now want to characterize the nature of slg (315) and elucidate the mechanism of cell cycle related changes in slg (315). H and L chains of slg (315) will be chemically characterized. Mono- and multi-valent DNP-carrier conjugates will be used for labeling DNP binding cells; cell cycle of labeled cells will be analyzed by microfluorimetry and flow cytometry. The effects of growth controls on the expression of antigen-binding receptors will be studied. We will investigate the mechanism of cell cycle dependent evasion from site-directed (slg-mediated) chemotherapy of myelomas.